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        <title>Environmental Health - Most accessed articles</title>
        <link>http://www.ehjournal.net</link>
        <description>The most accessed research articles published by Environmental Health</description>
        <dc:date>2010-02-26T00:00:00Z</dc:date>
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        <item rdf:about="http://www.ehjournal.net/content/8/1/2">
        <title>Mercury from chlor-alkali plants: measured concentrations in food product sugar</title>
        <description>Mercury cell chlor-alkali products are used to produce thousands of other products including food ingredients such as citric acid, sodium benzoate, and high fructose corn syrup. High fructose corn syrup is used in food products to enhance shelf life. A pilot study was conducted to determine if high fructose corn syrup contains mercury, a toxic metal historically used as an anti-microbial. High fructose corn syrup samples were collected from three different manufacturers and analyzed for total mercury. The samples were found to contain levels of mercury ranging from below a detection limit of 0.005 to 0.570 micrograms mercury per gram of high fructose corn syrup. Average daily consumption of high fructose corn syrup is about 50 grams per person in the United States. With respect to total mercury exposure, it may be necessary to account for this source of mercury in the diet of children and sensitive populations.</description>
        <link>http://www.ehjournal.net/content/8/1/2</link>
                <dc:creator>Renee Dufault</dc:creator>
                <dc:creator>Blaise LeBlanc</dc:creator>
                <dc:creator>Roseanne Schnoll</dc:creator>
                <dc:creator>Charles Cornett</dc:creator>
                <dc:creator>Laura Schweitzer</dc:creator>
                <dc:creator>Lyn Patrick</dc:creator>
                <dc:creator>Jane Hightower</dc:creator>
                <dc:creator>David Wallinga</dc:creator>
                <dc:creator>Walter Lukiw</dc:creator>
                <dc:source>Environmental Health 2009, 8:2</dc:source>
        <dc:date>2009-01-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-8-2</dc:identifier>
        <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2009-01-26T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ehjournal.net/content/4/1/6">
        <title>The Bhopal disaster and its aftermath: a review</title>
        <description>On December 3 1984, more than 40 tons of methyl isocyanate gas leaked from a pesticide plant in Bhopal, India, immediately killing at least 3,800 people and causing significant morbidity and premature death for many thousands more. The company involved in what became the worst industrial accident in history immediately tried to dissociate itself from legal responsibility. Eventually it reached a settlement with the Indian Government through mediation of that country&apos;s Supreme Court and accepted moral responsibility. It paid $470 million in compensation, a relatively small amount of based on significant underestimations of the long-term health consequences of exposure and the number of people exposed. The disaster indicated a need for enforceable international standards for environmental safety, preventative strategies to avoid similar accidents and industrial disaster preparedness.Since the disaster, India has experienced rapid industrialization. While some positive changes in government policy and behavior of a few industries have taken place, major threats to the environment from rapid and poorly regulated industrial growth remain. Widespread environmental degradation with significant adverse human health consequences continues to occur throughout India.</description>
        <link>http://www.ehjournal.net/content/4/1/6</link>
                <dc:creator>Edward Broughton</dc:creator>
                <dc:source>Environmental Health 2005, 4:6</dc:source>
        <dc:date>2005-05-10T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-4-6</dc:identifier>
        <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>4</prism:volume>
        <prism:startingPage>6</prism:startingPage>
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        <title>Obesity, physical activity, and the urban environment: public health research needs</title>
        <description>Persistent trends in overweight and obesity have resulted in a rapid research effort focused on built environment, physical activity, and overweight. Much of the focus of this research has been on the design and form of suburbs. It suggests that several features of the suburban built environment such as low densities, poor street connectivity and the lack of sidewalks are associated with decreased physical activity and an increased risk of being overweight. But compared to suburban residents, inner city populations have higher rates of obesity and inactivity despite living in neighborhoods that are dense, have excellent street connectivity and who&apos;s streets are almost universally lined with sidewalks.We suggest that the reasons for this apparent paradox are rooted in the complex interaction of land use, infrastructure and social factors affecting inner city populations. Sometimes seemingly similar features are the result of very different processes, necessitating different policy responses to meet these challenges. For example, in suburbs, lower densities can result from government decision making that leads to restrictive zoning and land use issues. In the inner city, densities may be lowered because of abandonment and disinvestment. In the suburbs, changes in land use regulations could result in a healthier built environment. In inner cities, increasing densities will depend on reversing economic trends and investment decisions that have systematically resulted in distressed housing, abandoned buildings and vacant lots.These varying issues need to be further studied in the context of the totality of urban environments, incorporating what has been learned from other disciplines, such as economics and sociology, as well as highlighting some of the more successful inner city policy interventions, which may provide examples for communities working to improve their health.Certain disparities among urban and suburban populations in obesity and overweight, physical activity and research focus have emerged that are timely to address. Comparable research on the relationship of built environment and health is needed for urban, especially inner city, neighborhoods.</description>
        <link>http://www.ehjournal.net/content/5/1/25</link>
                <dc:creator>Russell Lopez</dc:creator>
                <dc:creator>H. Patricia Hynes</dc:creator>
                <dc:source>Environmental Health 2006, 5:25</dc:source>
        <dc:date>2006-09-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-5-25</dc:identifier>
        <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>5</prism:volume>
        <prism:startingPage>25</prism:startingPage>
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        <item rdf:about="http://www.ehjournal.net/content/8/1/47">
        <title>The impact of transportation infrastructure on bicycling injuries and crashes: a review of the literature</title>
        <description>Background:
Bicycling has the potential to improve fitness, diminish obesity, and reduce noise, air pollution, and greenhouse gases associated with travel. However, bicyclists incur a higher risk of injuries requiring hospitalization than motor vehicle occupants. Therefore, understanding ways of making bicycling safer and increasing rates of bicycling are important to improving population health. There is a growing body of research examining transportation infrastructure and the risk of injury to bicyclists.
Methods:
We reviewed studies of the impact of transportation infrastructure on bicyclist safety. The results were tabulated within two categories of infrastructure, namely that at intersections (e.g. roundabouts, traffic lights) or between intersections on &quot;straightaways&quot; (e.g. bike lanes or paths). To assess safety, studies examining the following outcomes were included: injuries; injury severity; and crashes (collisions and/or falls).
Results:
The literature to date on transportation infrastructure and cyclist safety is limited by the incomplete range of facilities studied and difficulties in controlling for exposure to risk. However, evidence from the 23 papers reviewed (eight that examined intersections and 15 that examined straightaways) suggests that infrastructure influences injury and crash risk. Intersection studies focused mainly on roundabouts. They found that multi-lane roundabouts can significantly increase risk to bicyclists unless a separated cycle track is included in the design. Studies of straightaways grouped facilities into few categories, such that facilities with potentially different risks may have been classified within a single category. Results to date suggest that sidewalks and multi-use trails pose the highest risk, major roads are more hazardous than minor roads, and the presence of bicycle facilities (e.g. on-road bike routes, on-road marked bike lanes, and off-road bike paths) was associated with the lowest risk.
Conclusion:
Evidence is beginning to accumulate that purpose-built bicycle-specific facilities reduce crashes and injuries among cyclists, providing the basis for initial transportation engineering guidelines for cyclist safety. Street lighting, paved surfaces, and low-angled grades are additional factors that appear to improve cyclist safety. Future research examining a greater variety of infrastructure would allow development of more detailed guidelines.</description>
        <link>http://www.ehjournal.net/content/8/1/47</link>
                <dc:creator>Conor Reynolds</dc:creator>
                <dc:creator>M Anne Harris</dc:creator>
                <dc:creator>Kay Teschke</dc:creator>
                <dc:creator>Peter Cripton</dc:creator>
                <dc:creator>Meghan Winters</dc:creator>
                <dc:source>Environmental Health 2009, 8:47</dc:source>
        <dc:date>2009-10-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-8-47</dc:identifier>
        <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>47</prism:startingPage>
        <prism:publicationDate>2009-10-21T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ehjournal.net/content/9/1/8">
        <title>Air pollution and mortality in the Canary Islands: a time-series analysis</title>
        <description>Background:
The island factor of the cities of Las Palmas de Gran Canaria and Santa Cruz de Tenerife, along with their proximity to Africa and their meteorology, create a particular setting that influences the air quality of these cities and provides researchers an opportunity to analyze the acute effects of air-pollutants on daily mortality.
Methods:
From 2000 to 2004, the relationship between daily changes in PM10, PM2.5, SO2, NO2, CO, and ozone levels and daily total mortality and mortality due to respiratory and heart diseases were assessed using Generalized Additive Poisson models controlled for potential confounders. The lag effect (up to five days) as well as the concurrent and previous day averages and distributed lag models were all estimated. Single and two pollutant models were also constructed.
Results:
Daily levels of PM10, PM2.5, NO2, and SO2 were found to be associated with an increase in respiratory mortality in Santa Cruz de Tenerife and with increased heart disease mortality in Las Palmas de Gran Canaria, thus indicating an association between daily ozone levels and mortality from heart diseases. The effects spread over five successive days. SO2 was the only air pollutant significantly related with total mortality (lag 0).
Conclusions:
There is a short-term association between current exposure levels to air pollution and mortality (total as well as that due specifically to heart and respiratory diseases) in both cities. Risk coefficients were higher for respiratory and cardiovascular mortality, showing a delayed effect over several days.</description>
        <link>http://www.ehjournal.net/content/9/1/8</link>
                <dc:creator>Elena Lopez-Villarrubia</dc:creator>
                <dc:creator>Ferran Ballester</dc:creator>
                <dc:creator>Carmen Iniguez</dc:creator>
                <dc:creator>Nieves Peral</dc:creator>
                <dc:source>Environmental Health 2010, 9:8</dc:source>
        <dc:date>2010-02-12T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-9-8</dc:identifier>
        <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2010-02-12T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.ehjournal.net/content/9/1/10">
        <title>Maternal characteristics associated with the dietary intake of nitrates, nitrites, and nitrosamines in women of child-bearing age: a cross-sectional study</title>
        <description>Background:
: Multiple N-nitroso compounds have been observed in animal studies to be both mutagenic and teratogenic. Human exposure to N-nitroso compounds and their precursors, nitrates and nitrites, can occur through exogenous sources, such as diet, drinking water, occupation, or environmental exposures, and through endogenous exposures resulting from the formation of N-nitroso compounds in the body.  Very little information is available on intake of nitrates, nitrites, and nitrosamines and factors related to increased consumption of these compounds.MethodS: Using survey and dietary intake information from control women (with deliveries of live births without major congenital malformations during 1997-2004) who participated in the National Birth Defects Prevention Study (NBDPS), we examined the relation between various maternal characteristics and intake of nitrates, nitrites, and nitrosamines from dietary sources.  Estimated intake of these compounds was obtained from the Willet Food Frequency Questionnaire as adapted for the NBDPS. Multinomial logistic regression models were used to estimate odds ratios and 95% confidence intervals for the consumption of these compounds by self-reported race/ethnicity and other maternal characteristics.
Results:
: Median intake per day for nitrates, nitrites, total nitrites (nitrites + 5% nitrates), and nitrosamines was estimated at 40.48 mg, 1.53 mg, 3.69 mg, and 0.472 ug respectively. With the lowest quartile of intake as the referent category and controlling for daily caloric intake, factors predicting intake of these compounds included maternal race/ethnicity, education, body mass index, household income, area of residence, folate intake, and percent of daily calories from dietary fat. Non-Hispanic White participants were less likely to consume nitrates, nitrites, and total nitrites per day, but more likely to consume dietary nitrosamines than other participants that participated in the NBDPS. Primary food sources of these compounds also varied by maternal race/ethnicity.
Conclusions:
: Results of this study indicate that intake of nitrates, nitrites, and nitrosamines vary considerably by race/ethnicity, education, body mass index, and other characteristics.  Further research is needed regarding how consumption of foods high in nitrosamines and N-nitroso precursors might relate to risk of adverse pregnancy outcomes and chronic diseases.</description>
        <link>http://www.ehjournal.net/content/9/1/10</link>
                <dc:creator>John Grisenbeck</dc:creator>
                <dc:creator>Jean Brender</dc:creator>
                <dc:creator>Joseph Sharkey</dc:creator>
                <dc:creator>Michelle Steck</dc:creator>
                <dc:creator>John Huber</dc:creator>
                <dc:creator>Antonio Rene</dc:creator>
                <dc:creator>Thomas McDonald</dc:creator>
                <dc:creator>Paul Romitti</dc:creator>
                <dc:creator>Mark Canfield</dc:creator>
                <dc:creator>Peter Langlois</dc:creator>
                <dc:creator>Lucina Suarez</dc:creator>
                <dc:creator>National Birth Defects Prevention Study (nbdps)</dc:creator>
                <dc:source>Environmental Health 2010, 9:10</dc:source>
        <dc:date>2010-02-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-9-10</dc:identifier>
        <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>10</prism:startingPage>
        <prism:publicationDate>2010-02-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/9/1/9">
        <title>External costs of atmospheric Pb emissions: valuation of neurotoxic impacts due to inhalation</title>
        <description>Background:
The Impact Pathway Approach (IPA) is an innovative methodology to establish links between emissions, related impacts and monetary estimates. Only few attempts have so far been presented regarding emissions of metals; in this study the external costs of airborne lead (Pb) emissions are assessed using the IPA. Exposure to Pb is known to provoke impacts especially on children&apos;s cognition. As cognitive abilities (measured as IQ, intelligence quotient) are known to have implications for lifetime income, a pathway can be established leading from figures for Pb emissions to the implied loss in earnings, and on this basis damage costs per unit of Pb emission can be assessed.
Methods:
Different types of models are here linked. It is relatively straightforward to establish the relationship between Pb emissions and consequent increase in air-Pb concentration, by means of a Gaussian plume dispersion model (OML). The exposed population can then be modelled by linking the OML-output to population data nested in geo-referenced grid cells. Less straightforward is to establish the relationship between exposure to air-Pb concentrations and the resulting blood-Pb concentration. Here an Age-Dependent Biokinetic Model (ADBM) for Pb is applied. On basis of previous research which established links between increases in blood-Pb concentrations during childhood and resulting IQ-loss we arrive at our results.
Results:
External costs of Pb airborne emissions, even at low doses, in our site are in the range of 41-83 euro/kg emitted Pb, depending on the considered meteorological year. This estimate applies only to the initial effects of air-Pb, as our study does not address the effects due to the Pb environmental-accumulation and to the subsequent Pb re-exposure. These are likely to be between one and two orders of magnitude higher.
Conclusions:
Biokinetic modelling is a novel tool not previously included when applying the IPA to explore impacts of Pb emissions and related external costs; it allows for more fine-tuned, age-dependent figures for the external costs from low-dose exposure. Valuation of additional health effects and impacts e.g. due to exposure via ingestion appear to be feasible when extending the insights from the present pilot study.</description>
        <link>http://www.ehjournal.net/content/9/1/9</link>
                <dc:creator>Massimo Pizzol</dc:creator>
                <dc:creator>Marianne Thomsen</dc:creator>
                <dc:creator>Lise Marie Frohn</dc:creator>
                <dc:creator>Mikael Skou Andersen</dc:creator>
                <dc:source>Environmental Health 2010, 9:9</dc:source>
        <dc:date>2010-02-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-9-9</dc:identifier>
        <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>9</prism:startingPage>
        <prism:publicationDate>2010-02-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/9/1/11">
        <title>Perturbation of lipids and glucose metabolism associated with previous 2,4-D exposure: a cross-sectional study of NHANES III data, 1988-1994 </title>
        <description>Background:
Results from previous population studies showed that mortality rates from acute myocardial infarction and type-2 diabetes during the 1980s and 1990s in rural, agricultural counties of Minnesota, Montana, North and South Dakota, were higher in counties with a higher level of spring wheat farming than in counties with lower levels of this crop. Spring wheat, one of the major field crops in these four states, was treated for 85% or more of its acreage with chlorophenoxy herbicides.  In the current study NHANES III data were reviewed for associations of 2,4-dichlorophenoxy acetic acid (2,4-D) exposure, one of the most frequently used chlorophenoxy herbicides, with risk factors that are linked to the pathogenesis of acute myocardial infarction and type-2 diabetes, such as dyslipidemia and impaired glucose metabolism.
Methods:
To investigate the toxicity pattern of chlorophenoxy herbicides, effects of a previous 2,4-D exposure were assessed by comparing levels of lipids, glucose metabolism, and thyroid stimulating hormone in healthy adult NHANES III subjects with urinary 2,4-D above and below the level of detection, using linear regression analysis. The analyses were conducted for all available subjects and for two susceptible subpopulations characterized by high glycosylated hemoglobin (upper 50th percentile) and low thyroxine (lower 50th percentile).
Results:
Presence of urinary 2,4-D was associated with a decrease of HDL levels:  8.6% in the unadjusted data (p-value= 0.006), 4.8% in the adjusted data (p-value= 0.08), and 9% in the adjusted data for the susceptible subpopulation with low thyroxine (p-value= 0.02).  An effect modification of the inverse triglycerides-HDL relation was observed in association with 2,4-D.  Among subjects with low HDL, urinary 2,4-D was associated with increased levels of triglycerides, insulin, C-peptide, and thyroid stimulating hormone, especially in the susceptible subpopulations.  In contrast, subjects with high HDL did not experience adverse 2,4-D associated effects.
Conclusions:
The results indicate that exposure to 2,4-D was associated with changes in biomarkers that, based on the published literature, have been linked to risk factors for acute myocardial infarction and type-2 diabetes.</description>
        <link>http://www.ehjournal.net/content/9/1/11</link>
                <dc:creator>Dina Schreinemachers</dc:creator>
                <dc:source>Environmental Health 2010, 9:11</dc:source>
        <dc:date>2010-02-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-9-11</dc:identifier>
        <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>11</prism:startingPage>
        <prism:publicationDate>2010-02-26T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.ehjournal.net/content/4/1/17">
        <title>Teratogenicity of depleted uranium aerosols: A review from an epidemiological perspective</title>
        <description>Background:
Depleted uranium is being used increasingly often as a component of munitions in military conflicts. Military personnel, civilians and the DU munitions producers are being exposed to the DU aerosols that are generated.
Methods:
We reviewed toxicological data on both natural and depleted uranium. We included peer reviewed studies and gray literature on birth malformations due to natural and depleted uranium. Our approach was to assess the &quot;weight of evidence&quot; with respect to teratogenicity of depleted uranium.
Results:
Animal studies firmly support the possibility that DU is a teratogen. While the detailed pathways by which environmental DU can be internalized and reach reproductive cells are not yet fully elucidated, again, the evidence supports plausibility. To date, human epidemiological data include case examples, disease registry records, a case-control study and prospective longitudinal studies.DiscussionThe two most significant challenges to establishing a causal pathway between (human) parental DU exposure and the birth of offspring with defects are: i) distinguishing the role of DU from that of exposure to other potential teratogens; ii) documentation on the individual level of extent of parental DU exposure. Studies that use biomarkers, none yet reported, can help address the latter challenge. Thoughtful triangulation of the results of multiple studies (epidemiological and other) of DU teratogenicity contributes to disentangling the roles of various potentially teratogenic parental exposures. This paper is just such an endeavor.
Conclusion:
In aggregate the human epidemiological evidence is consistent with increased risk of birth defects in offspring of persons exposed to DU.</description>
        <link>http://www.ehjournal.net/content/4/1/17</link>
                <dc:creator>Rita Hindin</dc:creator>
                <dc:creator>Doug Brugge</dc:creator>
                <dc:creator>Bindu Panikkar</dc:creator>
                <dc:source>Environmental Health 2005, 4:17</dc:source>
        <dc:date>2005-08-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-4-17</dc:identifier>
        <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>4</prism:volume>
        <prism:startingPage>17</prism:startingPage>
        <prism:publicationDate>2005-08-26T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.ehjournal.net/content/9/1/7">
        <title>Consumer exposure to biocides - identification of relevant sources and evaluation of possible health effects</title>
        <description>Background:
Products containing biocides are used for a variety of purposes in the home environment. To assess potential health risks, data on products containing biocides were gathered by means of a market survey, exposures were estimated using a worst case scenario approach (screening), the hazard of the active components were evaluated, and a preliminary risk assessment was conducted.
Methods:
Information on biocide-containing products was collected by on-site research, by an internet inquiry as well as research into databases and lists of active substances. Twenty active substances were selected for detailed investigation. The products containing these substances were subsequently classified by range of application; typical concentrations were derived. Potential exposures were then estimated using a worst case scenario approach according to the European Commission&apos;s Technical Guidance Document on Risk Assessment. Relevant combinations of scenarios and active substances were identified. The toxicological data for these substances were compiled in substance dossiers. For estimating risks, the margins of exposure (MOEs) were determined.
Results:
Numerous consumer products were found to contain biocides. However, it appeared that only a limited number of biocidal active substances or groups of biocidal active substances were being used. The lowest MOEs for dermal exposure or exposure by inhalation were obtained for the following scenarios and biocides: indoor pest control using sprays, stickers or evaporators (chlorpyrifos, dichlorvos) and spraying of disinfectants as well as cleaning of surfaces with concentrates (hydrogen peroxide, formaldehyde, glutardialdehyde). The risk from aggregate exposure to individual biocides via different exposure scenarios was higher than the highest single exposure on average by a factor of three. From the 20 biocides assessed 10 had skin-sensitizing properties. The biocides isothiazolinone (mixture of 5-chloro-2-methyl-2H-isothiazolin-3-one and 2-methyl-2H-isothiazolin-3-one, CMI/MI), glutardialdehyde, formaldehyde and chloroacetamide may be present in household products in concentrations which have induced sensitization in experimental studies.
Conclusions:
Exposure to biocides from household products may contribute to induction of sensitization in the population. The use of biocides in consumer products should be carefully evaluated. Detailed risk assessments will become available within the framework of the EU Biocides Directive.</description>
        <link>http://www.ehjournal.net/content/9/1/7</link>
                <dc:creator>Stefan Hahn</dc:creator>
                <dc:creator>Klaus Schneider</dc:creator>
                <dc:creator>Stefan Gartiser</dc:creator>
                <dc:creator>Wolfgang Heger</dc:creator>
                <dc:creator>Inge Mangelsdorf</dc:creator>
                <dc:source>Environmental Health 2010, 9:7</dc:source>
        <dc:date>2010-02-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-069X-9-7</dc:identifier>
        <prism:publicationName>Environmental Health</prism:publicationName>
        <prism:issn>1476-069X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>7</prism:startingPage>
        <prism:publicationDate>2010-02-03T00:00:00Z</prism:publicationDate>
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